terone cypionate and initiate appropriate workup and management. long term clinical safety trials have not been conducted to assess the cardiovascular outcomes of testosterone replacement therapy in men. to date, epidemiologic studies and randomized controlled trials have been inconclusive for determining the risk of major adverse cardiovascular events (mace), such as non-fatal myocardial infarction, non fatal stroke, and cardiovascular death, with the use of testosterone compared to non-use. some studies, but not all, have reported an increased risk of mace in association with use of testosterone replacement therapy in men. patients should be informed of this possible risk when deciding whether to use or to continue to use testosterone cypionate injection. testosterone has been subject to abuse, typically at doses higher than recommended for the approved indication and in combination with other anabolic steroids. anabolic androgenic steroid abuse can lead to serious cardiovascular and psychiatric adverse reactions (see drug abuse and dependence). if testosterone abuse is suspected, check serum testosterone concentrations to ensure they are within therapeutic range. however, testosterone levels may be in the normal or subnormal range in men abusing synthetic testosterone derivatives. counsel patients concerning the serious adverse reactions associated with abuse of testosterone and anabolic steroids. conversely, consider the possibility of testosterone and anabolic steroid abuse in suspected patients who present with serious cardiovascular or psychiatric adverse events. edema, with or without congestive heart failure, may be a serious complication in patients with pre-existing cardiac, renal or hepatic disease. gynecomastia may develop and occasionally persists in patients being treated for hypogonadism. the preservative benzyl alcohol has been associated with serious adverse events, including the "gasping syndrome", and death in pediatric patients. although normal therapeutic doses of this product ordinarily deliver amounts of benzyl alcohol that are substantially lower than those reported in association with the "gasping syndrome", the minimum amount of benzyl alcohol at which toxicity may occur is not known. the risk of benzyl alcohol toxicity depends on the quantity administered and the liver and kidneys' capacity to detoxify the chemical. premature and low-birth weight infants may be more likely to develop toxicity. androgen therapy should be used cautiously in healthy males with delayed puberty. the effect on bone maturation should be monitored by assessing bone age of the wrist and hand every 6 months. in children, androgen treatment may accelerate bone maturation without producing compensatory gain in linear growth. this adverse effect may result in compromised adult stature. the younger the child the greater the risk of compromising final mature height. this drug has not been shown to be safe and effective for the enhancement of athletic performance. because of the potential risk of serious adverse health effects, this drug should not be used for such purpose.

e needed to induce pubertal changes and lower dosages can be used for maintenance after puberty. the chronological and skeletal ages must be taken into consideration, both in determining the initial dose and in adjusting the dose. for replacement in the hypogonadal male, 50 - 400 mg should be administered every two to four weeks. parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. warming and shaking the vial should redissolve any crystals that may have formed during storage at temperatures lower than recommended.

enous thromboembolism. miscellaneous: inflammation and pain at the site of intramuscular injection.

h rates, but may cause disproportionate advancement in bone maturation. use over long periods may result in fusion of the epiphyseal growth centers and termination of the growth process. androgens have been reported to stimulate production of red blood cells by enhancing production of erythropoietic stimulation factor. during exogenous administration of androgens, endogenous testosterone release is inhibited through feedback inhibition of pituitary luteinizing hormone (lh). at large doses of exogenous androgens, spermatogenesis may also be suppressed through feedback inhibition of pituitary follicle stimulating hormone (fsh). there is a lack of substantial evidence that androgens are effective in fractures, surgery, convalescence, and functional uterine bleeding. pharmacokinetics testosterone esters are less polar than free testosterone. testosterone esters in oil injected intramuscularly are absorbed slowly from the lipid phase; thus, testosterone cypionate can be given at intervals of two to four weeks. testosterone in plasma is 98 percent bound to a specific testosterone-estradiol binding globulin, and about 2 percent is free. generally, the amount of this sex-hormone binding globulin in the plasma will determine the distribution of testosterone between free and bound forms, and the free testosterone concentration will determine its half-life. about 90 percent of a dose of testosterone is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about 6 percent of a dose is excreted in the feces, mostly in the unconjugated form. inactivation of testosterone occurs primarily in the liver. testosterone is metabolized to various 17-keto steroids through two different pathways. the half-life of testosterone cypionate when injected intramuscularly is approximately eight days. in many tissues the activity of testosterone appears to depend on reduction to dihydrotestosterone, which binds to cytosol receptor proteins. the steroid-receptor complex is transported to the nucleus where it initiates transcription events and cellular changes related to androgen action.